Bee Venom Activates the Nrf2/HO-1 and TrkB/CREB/BDNF Pathways in Neuronal Cell Responses against Oxidative Stress Induced by Aβ
Autor: | Cong Duc, Nguyen, Jaehee, Yoo, Sun-Young, Hwang, Sung-Young, Cho, Myeonghun, Kim, Hyemin, Jang, Kyoung Ok, No, Jeong Cheol, Shin, Jae-Hong, Kim, Gihyun, Lee |
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Rok vydání: | 2021 |
Předmět: |
Male
Neurons Mice Inbred ICR Amyloid beta-Peptides NF-E2-Related Factor 2 Brain-Derived Neurotrophic Factor Membrane Proteins Apoptosis Neurodegenerative Diseases Peptide Fragments Bee Venoms Mice Oxidative Stress Neuroprotective Agents Gene Expression Regulation Animals Receptor trkB Cognitive Dysfunction Cyclic AMP Response Element-Binding Protein Heme Oxygenase-1 |
Zdroj: | International journal of molecular sciences. 23(3) |
ISSN: | 1422-0067 |
Popis: | Honeybee venom has recently been considered an anti-neurodegenerative agent, primarily due to its anti-inflammatory effects. The natural accumulation of amyloid-beta (Aβ) in the brain is reported to be the natural cause of aging neural ability downfall, and oxidative stress is the main route by which Aβ ignites its neural toxicity. Anti-neural oxidative stress is considered an effective approach for neurodegenerative therapy. To date, it is unclear how bee venom ameliorates neuronal cells in oxidative stress induced by Aβ. Here, we evaluated the neuroprotective effect of bee venom on Aβ-induced neural oxidative stress in both HT22 cells and an animal model. Our results indicate that bee venom protected HT22 cells against apoptosis induced by Aβ |
Databáze: | OpenAIRE |
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